Sodium Sensitivity in Normotensive and Borderline Hypertensive Humans

Sullivan, Jay M.; Prewitt, Russell L.; Ratts, Thomas E.

doi:10.1097/00000441-198804000-00025

Cited by 68 publications

(38 citation statements)

References 37 publications

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“…4 " 10 It has been observed that a larger proportion of both normotensive and hypertensive blacks are salt sensitive compared with similar whites for reasons that are unclear. 10 Thus, salt sensitivity is not a unique finding in blacks, although it does appear to be more prevalent compared with whites. Further, salt sensitivity does not seem to be unique to more affluent western cultures.…”

Section: (Hypertension 1991;17[suppl I]:i-115-i-121)mentioning

confidence: 97%

“…These trends include lower plasma renin activity 10 and a decreased responsiveness of the renin-angiotensin system after maneuvers that contract the circulating plasma volume 8 ; lower serum ionized calcium and higher serum magnesium levels have been observed to be associated with lower levels of plasma renin activity. 37 On the other hand, there appears to be a substantial overlap between salt-sensitive and salt-resistant subjects in these parameters.…”

Section: Mechanisms and Modifiers Of The Salt-bloodmentioning

confidence: 99%

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Racial and ethnic modifiers of the salt-blood pressure response.

et al. 1991

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The relation between sodium and blood pressure is a centuries-old question. A substantial body of epidemiological and experimental data has accumulated that strongly implicates NaCl as having a causal role in the genesis of arterial hypertension. Prospective studies that have been performed in diverse populations that have manipulated NaCl exposure by diet or infusion have repeatedly documented an NaCl pressor effect Further, similar studies in biracial populations have also demonstrated a greater prevalence of "salt sensitivity" in blacks compared with whites. The reasons for this observation are not entirely clear; however, intrinsic or hypertension-induced renal abnormalities that limit natriuretic capacity, reduced Na + ,K + -ATPase pump activity, other membrane ion transport disturbances, differential exposure to psychological stressors, greater insulin resistance, and dietary factors (reduced Ca + and K + intake) have all been suggested as possibly playing a role. Salt sensitivity appears to be a widespread phenomenon. However, it is critically important to determine what factors account for racial differences in salt sensitivity. Moreover, the prevalence of salt sensitivity in the general population is unknown. Current definitions of salt sensitivity are varied and unidirectional. In comparison with bidirectional criteria (blood pressure increase with salt loading and blood pressure decrease with salt restriction), they are probably inadequate to identify salt-sensitive individuals who manifest less extreme blood pressure change after dietary sodium or plasma volume manipulations. More sensitive criteria for diagnosing salt sensitivity will facilitate a better understanding of racial and ethnic differences in the prevalence of salt sensitivity. C ross-cultural studies support the concept that habitual NaCl intake is related to differences in mean blood pressure levels, hypertension prevalence, and the increasing slope of the blood pressure curve with advancing age among populations. -3 When considered in aggregate, different populations demonstrate a reasonably consistent relation among observed mean blood pressure, hypertension prevalence, and habitual sodium intake. In unacculturated societies consuming less than 50 meq/day sodium, hypertension is rare, blood pressures are low, there is little rise in blood pressure with advancing age, and blood pressures vary within a remarkably narrow range.2 On the other hand, in more developed societies in which sodium intake is From the Division of Epidemiology

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Section: (Hypertension 1991;17[suppl I]:i-115-i-121)mentioning

confidence: 97%

Section: Mechanisms and Modifiers Of The Salt-bloodmentioning

confidence: 99%

Racial and ethnic modifiers of the salt-blood pressure response.

et al. 1991

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“…Although the prevalence of "salt-sensitive" blood pressure in humans is not known, blood pressure tends to be more salt sensitive in hypertensive than in normotensive individuals, in blacks than in whites, and in older individuals. 1 ' 2 It has generally been assumed that salt sensitivity of blood pressure is related to dietary sodium intake; however, increasing evidence suggests that the anion ingested with sodium has an important impact on the subsequent blood pressure response. Recognition of the contribution of the anion to the development of NaCI-induced hypertension has practical implications as well as implications for understanding the mechanism by which a high dietary NaCI intake increases arterial pressure in the susceptible host.…”

Section: Brief Reviewmentioning

confidence: 99%

Relative contributions of dietary Na+ and Cl- to salt-sensitive hypertension.

Boegehold

1989

Hypertension

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The effect of dietary NaCI on blood pressure has generally been attributed to the sodium ion. However, recent evidence indicates that the anion accompanying sodium plays an important role in determining the magnitude of the blood pressure increase in response to a high dietary Intake of NaCI. The purpose of this review is to describe studies of blood pressure responses in several experimental models of salt-sensitive hypertension and in hypertensive humans to selective dietary sodium loading (without chloride) and to selective dietary chloride loading (without sodium). The full expression of salt sensitivity depends on high dietary intakes of both sodium and chloride. This observation has implications for understanding mechanisms contributing to NaCI-induced hypertension in the susceptible host. (Hypertension 1989;14:579-583) A high dietary intake of NaCI increases arterial pressure in several experimental models of hypertension and in both normotensive and hypertensive humans. Although the prevalence of "salt-sensitive" blood pressure in humans is not known, blood pressure tends to be more salt sensitive in hypertensive than in normotensive individuals, in blacks than in whites, and in older individuals.

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“…AN ABNORMALLY INCREASED BLOOD pressure-salt sensitivity is a common feature of essential hypertension, especially in African American patients (38). It is of substantial clinical and scientific interest to understand the mechanisms underlying the increase in blood pressure salt sensitivity.…”

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confidence: 99%

Renal medullary 11β-hydroxysteroid dehydrogenase type 1 in Dahl salt-sensitive hypertension

Liu

Singh

Usa

et al. 2008

Physiological Genomics

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Liu Y, Singh RJ, Usa K, Netzel BC, Liang M. Renal medullary 11␤-hydroxysteroid dehydrogenase type 1 in Dahl salt-sensitive hypertension. Physiol Genomics 36: 52-58, 2008. First published September 30, 2008 doi:10.1152/physiolgenomics.90283.2008.-The Dahl salt-sensitive rat is a widely used model of human salt-sensitive forms of hypertension. The kidney plays an important role in the pathogenesis of Dahl salt-sensitive hypertension, but the molecular mechanisms involved remain a subject of intensive investigation. Gene expression profiling studies suggested that 11␤-hydroxysteroid dehydrogenase type 1 might be dysregulated in the renal medulla of Dahl salt-sensitive rats. Additional analysis confirmed that renal medullary expression of 11␤-hydroxysteroid dehydrogenase type 1 was downregulated by a high-salt diet in SS-13 BN rats, a consomic rat strain with reduced blood pressure salt sensitivity, but not in Dahl salt-sensitive rats. 11␤-Hydroxysteroid dehydrogenase type 1 is known to convert inactive 11-dehydrocorticosterone to active corticosterone. The urinary corticosterone/11-dehydrocorticosterone ratio as well as urinary excretion of corticosterone was higher in Dahl salt-sensitive rats than in SS-13 BN rats. Knockdown of renal medullary 11␤-hydroxysteroid dehydrogenase type 1 with small-interfering RNA attenuated the early phase of salt-induced hypertension in Dahl salt-sensitive rats and reduced urinary excretion of corticosterone. Knockdown of 11␤-hydroxysteroid dehydrogenase type 1 did not affect blood pressure in SS-13 BN rats. Long-term attenuation of salt-induced hypertension was achieved with small hairpin RNA targeting renal medullary 11␤-hydroxysteroid dehydrogenase type 1. In summary, we have demonstrated that suppression of 11␤-hydroxysteroid dehydrogenase type 1 expression in the renal medulla attenuates salt-induced hypertension in Dahl salt-sensitive rats.

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Sodium Sensitivity in Normotensive and Borderline Hypertensive Humans

Cited by 68 publications

References 37 publications

Racial and ethnic modifiers of the salt-blood pressure response.

Racial and ethnic modifiers of the salt-blood pressure response.

Relative contributions of dietary Na+ and Cl- to salt-sensitive hypertension.

Renal medullary 11β-hydroxysteroid dehydrogenase type 1 in Dahl salt-sensitive hypertension

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